Basal ganglia damage and impaired visual function in the newborn infant

Visual performance and brain structures in the developing brain of pre-term infants

Visual Function Abnormalities and Prognosis in Eyes with Age-related Geographic Atrophy of the Macula and Good Visual Acuity

Effects of exercise on aspects of visual function

Summary Strenuous exercise has been reported to affect various aspects of visual and ocular function. In the first of two experiments, the effects of cycling, jogging and stair running on a range of visual functions were examined. None of these forms of exercise was found to have any significant effect on visual acuity, refractive error, dark focus, amplitude of accommodation or pupil size. Contrast sensitivity (CS), measured by an ascending method of limits (AML), was found to improve significantly after cycling and jogging but not after stair running. To investigate if the apparent improvement in CS was related to a change in ‘sensitivity’ or a change in decision criteria, CS was re‐measured before and after cycling using both the AML and a ‘criterion‐free’ method of constant stimuli (MOCS) procedure. Results obtained using the AML, confirmed the findings of the first experiment. However, results obtained using the MOCS procedure showed no significant change with exercise. This suggests that the improvement in CS found using the AML was due to a shift in subjects' decision criteria rather than a physiological change in ‘sensitivity’. It is argued that this change in decision criteria may be related to the positive mood changes which have been found to occur after exercise. This study demonstrates the importance of differentiating between changes in ‘sensitivity’ and changes in decision criteria especially where mood or motivation (and hence decision criteria) may be confounded with the independent variable. This is particularly important when evaluating the effects of exercise on visual function or evaluating the efficacy of vision training.

To compare the ability of 24-2 frequency-doubling perimetry (FDP-Matrix) with standard automated perimetry with the Swedish interactive threshold algorithm (SAP-SITA) in detection of visual function abnormalities in patients with glaucomatous-appearing optic discs (GAOD). This observational case-control study included 80 patients with GAOD and 54 control subjects diagnosed by masked assessment of optic disc stereoscopic photographs. Abnormal visual function at SAP-SITA and FDP-Matrix testing required consistent abnormalities in 2 visual field examinations, determined using the glaucoma hemifield test outside 99% normal limits, pattern standard deviation outside 95% normal limits, or 3 contiguous points in the pattern deviation probability plot outside 95% normal limits (at least 1 P<1%) within the same hemifield. The FDP-Matrix and SAP-SITA detected abnormal visual function in 51% and 44%, respectively, of GAOD eyes (P = .26), and both perimetry techniques identified 11% of healthy eyes as abnormal. Agreement between FDP-Matrix and SAP-SITA was moderate (kappa = 0.49), as only 35% of GAOD eyes and 2% of healthy eyes had both visual field test results flagged as abnormal. The FDP-Matrix detected abnormal visual function in more eyes with GAOD than did SAP-SITA, although this difference was not significant. Each visual field test tended to identify different subsets of eyes with GAOD as abnormal. Combination of these perimetry techniques may improve the detection of visual function abnormalities in patients with glaucoma.

Early assessment of visual function in preterm infants: How early is early?

1. Luis H. Ospina, MD* 1. *Assistant Professor, Pediatric Ophthalmology and Neuro-ophthalmology, Ste-Justine Hospital, University de Montreal, Montreal, Quebec, Canada After completing this article, readers should be able to: 1. Recognize cortical visual impairment (CVI) as an important cause of pediatric visual loss. 2. Identify the most frequent causes of pediatric CVI and, more specifically, understand the role of hypoxia as a cause of central visual damage. 3. Describe the different patterns and implications for future vision of hypoxic central visual damage occurring in preterm compared with term babies. 4. Know the clinical signs suggestive of CVI in children. 5. Discuss the involvement of visual functions other than visual acuity (ie, cognitive visual aspects) in CVI and correlate them with the likely affected neuroanatomic substrates. 6. Explain the value of using a multidisciplinary approach in rehabilitating children who have CVI early in their development. Vision loss caused by central nervous system damage often is referred to as CVI but also may be referred to as cerebral visual impairment or neurologic visual impairment. These terms refer to the fact that the primary defect may not necessarily be limited to the striate (primary visual) cortex and may affect other areas subserving vision, such as the visual associative cortex, optic radiations, and visual attention pathways. Although it is not yet certain which of these three terms best describes the visual deficit, it is clear that use of the label cortical blindness must be abandoned. That term not only evokes negative connotations for the child and the family but is inaccurate because in almost every instance, some degree of residual vision remains, and visual improvement can occur. CVI has become the greatest cause of pediatric visual impairment in developed countries (1)(2)(3)(4)(5) and is becoming increasingly prevalent in developing nations. CVI is a problem of increasing frequency for two primary reasons. First, the progress in neonatal care has resulted in improved survival of …

Numb deficiency impairs retinal structure and visual function in mice

Nondegenerative disorders involving the basal ganglia frequently do not present clinically as aprimary parkinsonian syndrome, but rather in the context of acute or subacute neurological symptoms such as altered level of consciousness, epileptic seizures, encephalopathy, or newly emerging hyperkinetic movement disorders. In these clinical scenarios, neuroimaging is often performed without aclear etiological hypothesis and primarily serves as an initial diagnostic orientation. Due to their end-arterial vascular supply, high metabolic demand, and central role within distributed motor and cognitive networks, the basal ganglia are particularly vulnerable to vascular, metabolic-toxic, inflammatory, and genetic insults. Accordingly, nondegenerative disorders often exhibit characteristic-and in some cases highly specific-patterns of involvement, the systematic analysis of which allows for rapid etiological stratification. This article provides astructured overview of the most relevant nondegenerative causes of movement disorders with basal ganglia involvement and describes typical neuroradiological patterns observed in vascular, metabolic-toxic, genetic, neoplastic, and infectious-inflammatory conditions. In addition, current developments in magnetic resonance imaging are discussed with respect to their potential and inherent limitations. Neuroradiological imaging remains acentral tool in the evaluation of nondegenerative movement disorders, guiding etiological classification, and directing further diagnostic work-up.

Event Abstract Back to Event The role of the cerebellum and basal ganglia in early Parkinson’s disease in motor timing prediction task: behavioral and fMRI study Martin Bareš1*, I. Husárová1, O.V Lungu2, R. Mareček1, M. Mikl1, T. Gescheidt1 and P. Krupa1 1 Masaryk University, Czechia 2 University of Montreal, Canada Objectives: Recently published studies demonstrated that the cerebellum and basal ganglia participate in motor timing tasks related to prediction. However, there is a debate as to the role played by these structures. To answer the question about exact role of the basal ganglia in predictive motor timing we studied patients with early Parkinson’s disease (PD) as a model of basal ganglia disorder. Methods: Using functional magnetic resonance imaging (fMRI), we tested the role of the cerebellum and BG in a dynamic timing prediction task that involved mediated interception of a moving target. The sample consisting of 20 patients with early PD (PD subjects) and 20 healthy age-matched healthy subjects (controls) performed a task in which they had to press a button to intercept a moving target on a computer screen. FMRI data were processed using SPM2. We considered three basic results for further evaluation – effect of hits, early errors, late errors – and their contrasts. The contrast hits minus all errors design was utilized to establish the comparison between PD subjects and controls. Results: The behavioral performance of the two sample groups on the timing prediction task was not found to be statistically significant. The fMRI analysis did not show the statistical significant difference in the activation in studied subcortical regions (PD subjects minus controls, hits minus all errors, p<0.05 FWE, corrected). Nevertheless, fMRI showed variability in regard to the location of brain activation during the task. While strong activity was found in the bilateral cerebellar lobes and the basal ganglia in controls, PD subjects showed increased activity in the basal ganglia only. Conclusion: These results stressed out the essential role of the cerebellum in motor timing prediction. The PD subjects seem to utilize different strategies and alternative functional circuits to maintain the same successful performance ratio. The basal ganglia involvement in predictive motor timing is inferior to the cerebellum. Supported by Research Project MSM0021622404. Conference: 10th International Conference on Cognitive Neuroscience, Bodrum, Turkey, 1 Sep - 5 Sep, 2008. Presentation Type: Oral Presentation Topic: Neuropsychiatric Disorders Citation: Bareš M, Husárová I, Lungu O, Mareček R, Mikl M, Gescheidt T and Krupa P (2008). The role of the cerebellum and basal ganglia in early Parkinson’s disease in motor timing prediction task: behavioral and fMRI study. Conference Abstract: 10th International Conference on Cognitive Neuroscience. doi: 10.3389/conf.neuro.09.2009.01.392 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 17 Dec 2008; Published Online: 17 Dec 2008. * Correspondence: Martin Bareš, Masaryk University, Brno, Czechia, martin.bares@fnusa.cz Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Martin Bareš I. Husárová O.V Lungu R. Mareček M. Mikl T. Gescheidt P. Krupa Google Martin Bareš I. Husárová O.V Lungu R. Mareček M. Mikl T. Gescheidt P. Krupa Google Scholar Martin Bareš I. Husárová O.V Lungu R. Mareček M. Mikl T. Gescheidt P. Krupa PubMed Martin Bareš I. Husárová O.V Lungu R. Mareček M. Mikl T. Gescheidt P. Krupa Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Age-related macular degeneration (AMD) affects various aspects of visual function compromising patients’ functional vision and quality of life. Compared to visual acuity, contrast sensitivity correlates better with vision-related quality of life and subjectively perceived visual impairment. It may also be affected earlier in the course of AMD than visual acuity. However, lengthy testing times, coarse sampling and resolution, and poor test–retest reliability of the existing contrast testing methods have limited its widespread adoption into routine clinical practice. Using active learning principles, the qCSF can efficiently measure contrast sensitivity across multiple spatial frequencies with both high sensitivity in detecting subtle changes in visual function and robust test–retest reliability, emerging as a promising visual function endpoint in AMD both in clinical practice and future clinical trials.

The aim of this study was to assess neuromotor function at school age in children who had cerebral infarction on neonatal magnetic resonance imaging (MRI). Twenty-two children with evidence of cerebral infarction on neonatal brain MRI (18 with arterial infarction and 4 with border-zone lesions) were assessed at school age with a structured neurologic examination and the Movement Assessment Battery for Children, a battery of tests designed to assess motor function. Of the 22 children, 6 (30%) had hemiplegia and a further 7 (30%) showed some neuromotor abnormality such as asymmetry on the neurologic examination (n = 4) or poor scores on the neuromotor test without any sign of asymmetry (n = 3). The remaining 9 children had a normal motor outcome. Hemiplegia was found only in children who had concomitant involvement of hemisphere, internal capsule, and basal ganglia on brain MRI. Children with involvement of the internal capsule, associated either with basal ganglia or hemispheric lesions, did not show hemiplegia but still had motor difficulties. Our results suggest that although hemiplegia occurs in a relatively small proportion of children with neonatal cerebral infarction, other signs of neuromotor impairment can be present, and these become more obvious at school age when a more specific assessment can be performed. These results also suggest that the involvement of the internal capsule on neonatal MRI can predict the presence of these abnormalities.

Cysticercosis lesions in basal ganglia are common but clinically silent

Only one large series using statistical parametric mapping (SPM) reports on FDG-PET in sporadic (Heidenhain and non-Heidenhain variant) Creutzfeldt-Jakob disease (sCJD), describing hypometabolism in bilateral parietal, frontal, and occipital cortices. Our aim was to study FDG-PET in non-Heidenhain probable sCJD patients in order to assess the most pertinent FDG-PET pattern, and to compare FDG-PET and MRI data. We used both SPM and NeuroGam(®) software analysis, compared with healthy controls, to describe the FDG-PET abnormalities. Individual FDG-PET and MRI-DWI data were compared. SPM group analysis showed lateralized hypometabolism in the medial parietal cortex, the lateral and medial frontal (sparing Brodmann's area 4 and 6 and the anterior cingulate cortex), and lateral parietal cortex, in the absence of basal ganglia or cerebellar hypometabolism. The most severe hypometabolism was seen in Brodmann's area 31, and to a lesser degree area 23 (both areas correspond to the posterior cingulate cortex) and the precuneus. On individual analysis using NeuroGam(®) software, additional variable temporal cortex and frequent basal ganglia (with caudate nucleus as the most frequently involved structure) hypometabolism was seen, in the absence of cerebellar hypometabolism. The cerebral lobe cortex was more frequently and more severely hypometabolic than basal ganglia structures. Concordance between FDG-PET and MRI abnormalities was most often present for both the cerebral lobe cortex and the basal ganglia. In the case of discordance, FDG-PET was more sensitive than MRI for the cortex, whereas MRI was more sensitive than FDG-PET for the basal ganglia. When pathological, both cortical lobe cortex and basal ganglia involvement were slightly more often lateralized on FDG-PET than on MRI. Despite the presence of overlapping features with other diseases presenting with rapidly progressive dementia, the FDG-PET pattern we found in our non-Heidenhain sCJD patients may help in the differential diagnosis of rapidly progressive dementia.

Leigh syndrome is a rare progressive neurodegenerative disease with variable clinical presentations associated with mitochondrial dysfunction. However, the most common presentations are motor and intellectual developmental delays, with signs and symptoms of brainstem and basal ganglia involvement. We describe a 6-year-old boy with a history of delayed developmental milestones who presen-ted to our hospital due to unconscious status and respiratory distress syndrome. The patient underwent brain magnetic resonance imaging (MRI), and multiple subacute necrotic lesions were identified at the bilateral basal ganglia, thalamus, cerebral peduncles, brainstem, and cortical regions. DNA analysis was performed, which revealed muta-tions in SURF1. The patient experienced several relapses and died of respiratory failure and hospital-acquired infections, 3 years after the diagnosis of Leigh syndrome. Leigh syndrome should be considered in children with neurological problems and bilateral basal ganglia or brainstem abnormalities. Neurological MRI can be useful for guiding clinicians in ordering the most appropriate enzymatic and genetic analyses for further diagnosis.